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Helicobacter pylori and peptic ulcer in cirrhotic patients

October 2008

October 2008
24(6):849-852

Authors:

Tehran University of Medical Sciences

Objective: H.pylori infection increases the risk of peptic ulcer in cirrhotic patients. The role of H.pylori in inducing peptic ulcer disease in chronic liver disease patients remains controversial. The objective was to see if etiology of peptic ulcer in cirrhotic patients is related to H.pylori infection. Methodology: Sixty cirrhotic patients were enrolled in the study. Peptic ulcer was detected in patients by means endoscope. Sera from patients were tested for Helicobacter pylori antibodies by a commercial ELISA kit. t student and fisher test was used for statistical analysis. Results: Active peptic ulcer was detected in nine cirrhotic patients. Of the nine patients with peptic ulcer eight (88.9%) tested positive for Helicobacter pylori antibodies and of the remaining 51 patients, 31(60.8%) tested positive for Helicobacter pylori antibodies. Conclusion: Helicobacter pylori infections in our series of cirrhotic patients with peptic ulcer seems to show the same pattern as described in cirrhotic patients without peptic ulcer (P=0.078). The suggestion that the etiology of the peptic ulcer in cirrhotic patients could be related to Helicobacter pylori infection was not confirmed by our study.

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Pak J Med Sci 2008 Vol. 24 No. 6 www.pjms.com.pk 849

Original Article

HELICOBACTER PYLORI AND PEPTIC

ULCER IN CIRRHOTIC PATIENTS

Monireh Rahimkhani1, Hadi Ghofrani2

ABSTRACT

Objective: H.pylori infection increases the risk of peptic ulcer in cirrhotic patients.

The role of H.pylori in inducing peptic ulcer disease in chronic liver disease patients remains

controversial. The objective was to see if etiology of peptic ulcer in cirrhotic patients is related

to H.pylori infection.

Methodology: Sixty cirrhotic patients were enrolled in the study. Peptic ulcer was detected in

patients by means endoscope. Sera from patients were tested for Helicobacter pylori antibodies

by a commercial ELISA kit. t student and fisher test was used for statistical analysis.

Results: Active peptic ulcer was detected in nine cirrhotic patients. Of the nine patients with

peptic ulcer eight (88.9%) tested positive for Helicobacter pylori antibodies and of the remaining

51 patients, 31(60.8%) tested positive for Helicobacter pylori antibodies.

Conclusion: Helicobacter pylori infections in our series of cirrhotic patients with peptic ulcer

seems to show the same pattern as described in cirrhotic patients without peptic ulcer (P=0.078).

The suggestion that the etiology of the peptic ulcer in cirrhotic patients could be related to

Helicobacter pylori infection was not confirmed by our study.

KEY WORDS: H.pylori, Peptic ulcer, Cirrhosis.

Pak J Med Sci October - December 2008 (Part-II) Vol. 24 No. 6 849-852

How to cite this article:

Rahimkhani M, Ghofrani H. Helicobacter pylori and peptic ulcer in cirrhotic patients. Pak J Med

Sci 2008;24(6):849-52.

1. Monireh Rahimkhani MD, Ph.D

Faculty of Allied of Medical Sciences,

Tehran University of Medical Sciences,

Ghods st, Poorsina st,

Tehran, Iran.

2. Hadi Ghofrani, MD, Ph.D

Department of Gastroentrology and Endoscopy,

Emam Hospital,

Tehran, Iran.

Correspondence

Monireh Rahimkhani,

E-mail: rrahimkhani@sina.tums.ac.ir

* Received for Publication: May 8, 2008

* Revision Received: August 8, 2008

* Revision Accepted: August 18, 2008

INTRODUCTION

Helicobacter pylori(H.pylori) is established as

an important etiologic factor for chronic gas-

tritis and peptic ulcer diseases.1 Eradication of

H.pylori gastric infection markedly decreases

peptic ulcer recurrence in patients.2-8 Moreover,

cure of H.pylori infection decreases the risk of

recurrence in patients with bleeding peptic

ulcer.3

Factors related to peptic ulcer development

and the causes of increased prevalence of the

disease in cirrhotic patients are poorly under-

stood. Patients with liver cirrhosis are fre-

quently subjected to a number of disorders of

the gastric mucosa. Peptic lesions in the

gastroduodonal mucosa have been found to be

more frequent in cirrhotic than in control.4

A previous report indicates that H.pylori

infection increases the risk of peptic ulcer in

cirrhotic patients by 2.7 fold; however, subse-

quent study does not confirm this finding.5

Some studies have reported that there is some

850 Pak J Med Sci 2008 Vol. 24 No. 6 www.pjms.com.pk

Monireh Rahimkhani et al.

degree of difference between the hepatic pres-

sure gradient in patients with and without

gastric ulcer.6 Thus the role of H.pylori in in-

ducing peptic ulcer disease in chronic liver dis-

ease patients remains controversial.7 This study

was conducted to see if etiology of peptic ulcer

in cirrhotic patients is related to H.pylori

infection.

METHODOLOGY

Sixty cirrhotic patients between July 2006

and March 2008 were enrolled in the study. A

diagnosis of cirrhosis was made on the basis of

clinical findings, abdominal sonogram; endo-

scopic procedures done by fellows in

gasteroenterology besides laboratory param-

eters and/or liver biopsy. At the time of inclu-

sion a questionnaire was completed and pa-

tient serum was obtained and stored at -70oC

until analyzed. Etiology of the cirrhosis was

defined as viral when HBS Ag or antibodies to

the hepatitis C virus were present. Less com-

mon diseases such as alcoholic cirrhosis, Wil-

son disease, primary billiary cirrhosis, cancer

and autoimmune was detected. According to

the current clinical criteria. Cancer in these

patients was etiological factor for cirrhosis.

Finally some patients were defined as

unknown etiology of cirrhosis.

Sera from patients were tested for

Helicobacter pylori antibodies by a commer-

cial ELISA kit (PISHTAZ TEB). Its sensivity for

the diagnosis of Helicobacter pylori infection

has been reported to be >98% and its specific-

ity >98. In accordance with the manufactur-

ers’ instructions, ELISA values lower than 15

were considered negative and values 15 or over

positive.

Statistical Analysis: Statistical analyses were

performed with independent students t test

and chi-square test accordingly. Results were

considered statistically significant at P<0.05.

RESULTS

A total sixty cirrhotic patients who attended

the gastrointestinal clinic during twenty month

study period were enrolled in the study. Thirty

eight patients were male and twenty two

female with mean age+-sd, 47.22+-17.12(15-

72) years. Table-I shows the age, sex and etiol-

ogy of patients.

Active peptic ulcer was detected in nine cir-

rhotic patients by means endoscope (model

GFI-XQ230). Of the nine patients with peptic

ulcer eight (88.9%) tested positive for

Helicobacter pylori antibodies and of the re-

maining 51 patients, thirty one (60.8%) tested

positive for Helicobacter pylori antibodies

(Table-II). Peptic ulcer was detected in

anterum, fundus and duodenal area.

Esophageal varices were diagnosed in 13 of

the 60 patients by means endoscope. Of the 13

patients with esophageal varices eleven (84.6%)

tested positive for Helicobacter pylori antibod-

ies and of the remaining 47 patients, twenty

eight (59.6%) tested positive for Helicobacter

pylori antibodies (Table-III).

Table-I: Results of the univariate analysis

Analysis Number %

Sex Male 38 63.3

Female 22 36.7

Total 60 100

Age <20 6 10

21-30 8 13.4

31-40 6 10

41-50 14 23.3

51-60 11 18.3

>60 15 25

Total 60 100

Cirrhosis

etiology

Alcoholic 2 3.3

HCV 6 10

HBV 16 26.7

Primary 3 5

billiary

cirrhosis

Wilson 1 1.7

Cancer 5 8.3

Autoimmune 1 1.7

Unknown 24 40

Total 60 100

DISCUSSION

There are many factors that could have in-

duced peptic ulcer. As regards gastric acidity

in cirrhosis, there was marked hypogastric

acidity over the entire circadian cycle which

was evaluated from 24-h gastric acidity. Nev-

ertheless, the actual mechanism of hypoacid-

ity is poorly understood. The degree of acidity

and modulators of gastric mucosal response

needs further investigation to confirm its asso-

ciation with the pathogenesis of peptic ulcer

in cirrhosis.5 The most important etiology of

peptic ulcer is H.pylori infection. But the etiol-

ogy of cirrhosis was not related to the

seroprevalence of Helicobacter pylori infection

and on the other hand Helicobacter pylori

infection was not related to sex, age and

etiology of cirrhosis.

Peptic ulcer is a major problem in patients

with liver cirrhosis and the risk of the peptic

ulcer is greater in these patients.7 Prospective

endoscopic surveys have shown the incidence

of peptic ulcer of 4.3% in patients with cirrho-

sis which is between 20 and 47 times greater

than in the general population.7

It has been demonstrated that patients with

liver cirrhosis are frequently subjected to a

number of disorders of the gastric mucosa

which have been observed more often in cir-

rhotic patients than in controls. Helicobacter

pylori infection is also an important factor in

the pathogenesis of peptic ulcer.9 But H.pylori

eradication does not protect all cirrhotics from

ulcer recurrence.10

The prevalence of peptic ulcer observed in

this study is 15% of total 60 cirrhotic patients

more than previous studies).

Our results demonstrate that, H.pylori

infection was an independent factor associated

with cirrhosis and peptic ulcer. The difference

in the prevalence of H.pylori infection between

cirrhotic patients with peptic ulcer (88.9%) and

without peptic ulcer (51.7%) did not reach

statistical significance (P=0.078).

Esophageal varicies and variceal bleeding is

most related to death in cirrhotic patients.

There seems to exist associations between in-

fection and other complications such as mal-

nutrition, hepatic encephalopathy and variceal

bleeding.11,12 In this study we obtained the same

results about relationship between esophageal

varicies and H.pylori infection. The difference

in the prevalence of H.pylori infection between

cirrhotic patients with esophageal varicies

(84.6%) and without esophageal varicies

(59.6%) did not reach statistical significance

(P=0.078).

In conclusion, Helicobacter pylori infections

in our series of cirrhotic patients with peptic

ulcer seems to show the same pattern as

described in cirrhotic patients without peptic

ulcer (P=0.078). The suggestion that the etiol-

ogy of the peptic ulcer in cirrhotic patients

Pak J Med Sci 2008 Vol. 24 No. 6 www.pjms.com.pk 851

H. Pylori & peptic ulcer in crirrhotic patients

Table-III: Esophageal varicies and H.pylori IgG in cirrhotic patients

Esophageal varicies IgG Negative Positive Total

Positive 28(59.6%) 11(84.6%) 39(100%)

Negative 19(40.4%) 2(15.4%) 21(100%) X =3.109

Total 47(100%) 13(100%) 60(100%) P=0.078

Table-II: Peptic ulcer and H.pylori IgG in cirrhotic patients

Peptic ulcer IgG Negative Positive Total

Positive 31(60.8%) 8(88.9%) 39(100%)

Negative 20(39.2%) 1(11.1%) 21(100%) X =3.105

Total 51(100%) 9(100%) 60(100%) P=0.078

852 Pak J Med Sci 2008 Vol. 24 No. 6 www.pjms.com.pk

could be related to Helicobacter pylori infec-

tion was not confirmed by our study. This

study was carried out in only one centre so the

study patients may not represent all cirrhotic

patients. Therefore, more studies performed in

other regions with more patients are needed

to confirm our findings.

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Article

Apr 2001

An increased risk for gastric cancer in patients with liver cirrhosis has recently been reported. This study was performed in order to determine gastric epithelial cell proliferation in cirrhotic patients and to evaluate the role of congestive gastropathy (CG) and Helicobacter pylori infection in this process. Thirty-six cirrhotic patients and 18 controls were enrolled in the study. All patients underwent endoscopy and three biopsies were performed in the antrum and three in the gastric body. The presence of H. pylori infection was assessed by a rapid urease test and histology. The antral biopsies were used for gastric cell proliferation assessment by an immunohistochemical analysis (Ki-67). There was no significant difference in epithelial cell proliferation between cirrhotics and controls. Gastric proliferation values were higher in patients with H. pylori infection compared with uninfected patients, both in cirrhotic (P = 0.003) and in control groups (P = 0.06). Among the cirrhotic group, we found a progressive increase in gastric cell proliferation values related to the degree of CG, the highest values being observed in cirrhotic patients with severe CG. Moreover, cirrhotics with both severe CG and H. pylori infection had the highest proliferation values when compared with all other subgroups. In conclusion, this study found that: (1) CG significantly affects epithelial cell proliferation in gastric mucosa in cirrhotic patients, (2) H. pylori infection plays a similar role in gastric cell proliferation in both cirrhotic and non-cirrhotic patients, and (3) CG and H. pylori could act synergistically in this process.

Helicobacter pylori is a risk factor for peptic ulcer disease in cirrhotic patients. A meta-analysis

Article

Aug 2002
EUR J GASTROEN HEPAT

Peptic ulcer disease is highly prevalent in cirrhosis, and ulcer complications are a major cause of morbidity in these patients. Helicobacter pylori infection is considered the chief aetiological factor of ulcer disease. However, in cirrhotic patients the role of H. pylori in the pathogenesis of peptic ulcer remains uncertain. To evaluate the evidence of the pathogenic role of H. pylori infection in peptic ulcer disease in patients with cirrhosis. An extensive MEDLINE search of the literature was performed. Studies reporting the prevalence of H. pylori infection in cirrhotic patients with and without ulcers were selected. Meta-analysis was conducted using RevMan 4.0.3. Pooled odds ratios were calculated for each comparison, using a fixed model analysis. The search identified seven studies with a total of 976 patients with cirrhosis (275 cases with ulcer disease and 701 controls). The prevalence of H. pylori infection in patients with peptic ulcer disease was higher than in those without. The pooled odds ratio was 2.70 (95% CI, 1.91-3.82). H. pylori infection was associated more or less equally with duodenal and gastric ulcers. H. pylori infection increases the risk of peptic ulcer disease in patients with cirrhosis.

Correlations of portal hypertensive gastropathy of hepatitis B cirrhosis with other factors

Article

Nov 2002
HEPATOB PANCREAT DIS

To study the clinical relations of portal hypertensive gastropathy (PHG) of hepatitis B cirrhosis to other factors. Three groups of subjects were studied prospectively at our hospital from March 2000 to March 2001: 159 hepatitis B cirrhotic patients with portal hypertension, 114 hepatitis B cirrhotic patients without portal hypertension, and 97 control subjects. Free portal vein pressure (FPP) was measured during surgery. Liver function was assessed by Pugh's modification of Child's criteria. The area of liver collagen fibrin was studied using color image analysis system. Esophageal varices were identified by Dagradi grading. Gastric varices were identified according to Northern Italian Endoscopic Council (NIEC) grading. Hypersplenism was assessed with the reduction of WBC, HGB and PLT. Hepatitis B virus in the gastric mucosa was detected by immunizing histochemistry. Helicobacter pylori (H. pylori) organisms were identified by rapid urease testing and/or examination of the stained biopsy specimens (haematoxylin and eosin). To analyze the correlation between these endoscopic signs at the gastric level and other factors. The differences of FPP among the three groups (patients with grade I, II, and III gastropathy) were not significant. There was no correlation between Child-Pugh classification grading and the severity of gastropathy (P=0.153). The differences of the area of liver collagen fibrin among the three grade gastropathy were not statistically significant (P=0.801). There was a significant difference in the prevalence of severe PHG among grade I, II, III, IV and V esophageal varices (P<0.001). PHG was present in a similar percentage of patients with gastric varices compared with those without gastric varices (P=0.209). There was a significant difference in the severity between PHG and hypersplenism (P=0.003). Seven patients with PHG had no microscopic evidence of hepatitis B virus infection in the gastric wall. There was no correlation between Child-Pugh classification grading and infection of H. pylori (P=0.7491). The most important element causing PHG is the increased portal pressure as a prerequisite. In addition, other factors may contribute to the development of PHG. PHG often occurs in patients with the presence of esophageal varices. There is a marked correlation between the severity of PHG and hypersplenism. Hepatitis B virus and H. pylori infection are unlikely to be involved in the pathogenesis of PHG. The development of PHG is less influenced either by the severity of liver disease (Child-Pugh grade) and cirrhosis or by the presence or non presence of gastric varices.

Cirrhosis and Bacterial Infections

Article

Jan 2004
Rom J Gastroenterol

Hendrik Vilstrup

Half of cirrhosis patients die within two years after diagnosis, in most cases from cirrhosis related causes; most frequently variceal bleeding closely followed by infections. There seems to exist associations between infection and other complications such as malnutrition, hepatic encephalopathy and variceal bleeding. Cirrhosis patients have an acquired immune deficiency because of dyshomeostasis and malnutrition. All host defence systems are compromised, e.g. the acute phase response, and macrophage, neutrocyte, and lymphocyte functions. Simultaneously, there is increased microbiotic invasion, due to increased nosocomial exposure, intestinal translocation, aspiration, skin lesions, and trauma. Compared to the background population, the mortality of infections is more than 20 times increased in cirrhosis. The incidence of peritonitis, bacteremia, urinary tract infection, pneumonia, meningitis, tuberculosis, liver abscess is increased more than tenfold, and the mortality of each episode 3-10 times higher. The systemic response and accompanying classical symptoms are usually weakened. When positive isolates can be obtained the flora tends to be of an opportunistic nature. Infection should be suspected in any cirrhotic patient with an unexpected deterioration of clinical course. Treatment should be started on suspicion and with large dose broad-spectrum antibiotics (avoiding aminoglycosides). Antibiotic prophylaxis is efficacious at variceal bleeding, recurrent peritonitis, and at very low protein ascites, but otherwise is associated with risk of infection with multi-resistant strains.

[Liver cirrhosis and bacterial infections]

Article

Mar 2005
Ugeskr Laeger

Hendrik Vilstrup

The mortality rate of infections in patients with cirrhosis is more than 20 times that in the general population. Both the host's defense system and the systemic response to infection are compromised, and the microbiotic invasion, often of an opportunistic nature, is augmented due to intestinal translocation, aspiration, and other factors. Infection should be suspected in any cirrhotic patient with a deteriorating clinical course, and treatment with large doses of broad-spectrum antibiotics, avoiding aminoglycosides, should be promptly initiated. Antibiotic prophylaxis carries a high risk of colonization with resistant strains but reduces the mortality rate from upper gastrointestinal bleeding and recurrent spontaneous bacterial peritonitis.

Factors predisposing to peptic ulcer disease in asymptomatic cirrhotic patients

Article

Jul 2005

There is a high prevalence of peptic ulcer in cirrhotic patients, but the pathogenesis of peptic ulcer in cirrhosis remains inconclusive. To investigate factors associated with peptic ulcer and to evaluate peptic ulcer prevalence in asymptomatic cirrhotic patients. A total of 130 cirrhotics were recruited into the study for endoscopic screening. Data were collected and biochemical tests were done. Doppler ultrasound was used to assess the portal vein velocity and size. Patients underwent endoscopy for the presence of varices and peptic ulcer. Helicobacter pylori infection was confirmed by urease test, histology and 14C-urea breath test. Statistical analysis was performed. Peptic ulcer was detected in 50 (39%) cases. Between peptic ulcer and non-peptic ulcer groups, there were no significant differences in age, sex, alcoholic drinking, smoking, non-steroidal anti-inflammatory drug use, portal vein velocity and size, except for H. pylori infection (P = 0.006), serum albumin (P = 0.02) and Child-Pugh score (P = 0.03). By multivariate analysis, H. pylori infection (OR: 3.26; 95% CI: 1.49-7.13; P = 0.003), Child-Pugh classes B (OR: 2.48; 95% CI: 1.04-5.91; P = 0.04) and C (OR: 3.26; 95% CI: 1.2-8.81; P = 0.02) were independently associated with peptic ulcer. H. pylori infection and advanced cirrhosis are important factors associated with active peptic ulcer.